The contractile, hemodynamic and coronary effects of acute cigarette smoking were investigated clinically in 9 patients with coronary heart disease confirmed by coronary angiography. Immediately after smoking a cigarette (0.8 mg nicotine, 13 mg condensate) there were significant increases in the cardiac output and contractility of the left ventricle. Cigarette smoking therefore leads to an acute rise in ventricular function and especially to an increase in contractility in relation to velocity. Coronary circulation and myocardial oxygen consumption rise in accordance with the change in ventricular dynamic and hemodynamic stress factors. Smoking cigarettes appears to have little effect on the pharmacologically demonstrable coronary reserve of the left ventricle. In the isolated ventricular myocardium nicotine produced a significant positive inotropic effect with corresponding increases in the contraction and contraction velocity, whereas the relaxation velocity remained unchanged. Whether there is a connection between the rise in inotropy demonstrable in the isolated ventricular myocardium and the rise in contractility is still undecided.